Proximity to Major Roads and Risks of Childhood Recurrent Wheeze and Asthma in a Severe Bronchiolitis Cohort

Air pollution exposures have been suggested as risk factors for childhood respiratory diseases. We investigated proximity to major roads, an indicator of air pollution exposure, and its associations with childhood recurrent wheeze and asthma. We used data from a multicenter prospective cohort study of 921 infants hospitalized for bronchiolitis and recruited from 14 U.S. states. Primary exposure was residential proximity to the nearest major road at birth through age 3 years. Residential distance from nearest major road was divided into four categories: <100, 100–200, 201–300, and >300 m. Outcomes were parent-reported recurrent wheeze by age 3 years and asthma by age 5 years. Associations between residential proximity to major roads and respiratory outcomes were investigated using multivariable Cox proportional hazards modeling and logistic regression, adjusted for confounders. Out of 920 participants with home address data, pooled estimates identified 241 (26%) participants resided within 300 m of a major road, 296 (32%) developed recurrent wheeze by age 3, and 235 out of 858 participants (27%) developed asthma by 5 years. Participants who resided close to a major road had the highest risk of recurrent wheeze (adjusted hazards ratio for <100 m, 1.59, 95%CI: 1.08–2.33) and asthma (adjusted odds ratio for 201–300 m, 1.62, 95%CI: 1.16–2.25), compared to those residing >300 m from a major road. Proximity to major roads is associated with increased risks of recurrent wheeze and asthma in young children.

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Air Pollution Is Associated with Cognitive Deterioration of Alzheimer’s Disease

Gerontology ◽

10.1159/000515162 ◽

2021 ◽

pp. 1-9

Author(s):

Feng Cheng Lin ◽

Chih Yin Chen ◽

Chung Wei Lin ◽

Ming Tsang Wu ◽

Hsuan Yu Chen ◽

...

Keyword(s):

Risk Factors ◽

Air Pollution ◽

Social Engagement ◽

Proportional Hazards ◽

Cox Proportional Hazards ◽

Rank Test ◽

Cognitive Deterioration ◽

Clinical Dementia Rating ◽

Severe Stage ◽

Increased Risk

Introduction: Dementia is one of the major causes of disability and dependency among older people worldwide. Alzheimer’s disease (AD), the most common cause of dementia among the elderly, has great impact on the health-care system of developed nations. Several risk factors are suggestive of an increased risk of AD, including APOE-ε4, male, age, diabetes mellitus, hypertension, and low social engagement. However, data on risk factors of AD progression are limited. Air pollution is revealed to be associated with increasing dementia incidence, but the relationship between air pollution and clinical AD cognitive deterioration is unclear. Methods: We conducted a case-control and city-to-city study to compare the progression of AD patients in different level of air-polluted cities. Clinical data of a total of 704 AD patients were retrospectively collected, 584 residences in Kaohsiung and 120 residences in Pingtung between 2002 and 2018. An annual interview was performed with each patient, and the Clinical Dementia Rating score (0 [normal] to 3 [severe stage]) was used to evaluate their cognitive deterioration. Air pollution data of Kaohsiung and Pingtung city for 2002–2018 were retrieved from Taiwan Environmental Protection Administration. Annual Pollutant Standards Index (PSI) and concentrations of particulate matter (PM10), sulfur dioxide (SO2), ozone (O3), nitrogen dioxide (NO2), and carbon monoxide (CO) were obtained. Results: The PSI was higher in Kaohsiung and compared with Pingtung patients, Kaohsiung patients were exposed to higher average annual concentrations of CO, NO2, PM10, and SO2. AD patients living in Kaohsiung suffered from faster cognitive deterioration in comparison with Pingtung patients (log-rank test: p = 0.016). When using multivariate Cox proportional hazards regression analysis, higher levels of CO, NO2, PM10, and SO2 exposure were associated with increased risk of AD cognitive deterioration. Among all these air pollutants, high SO2 exposure has the greatest impact while O3 has a neutral effect on AD cognitive deterioration. Conclusions: Air pollution is an environment-related risk factor that can be controlled and is associated with cognitive deterioration of AD. This finding could contribute to the implementation of public intervention strategies of AD.

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Air pollution and mortality in a large, representative U.S. cohort: multiple-pollutant analyses, and spatial and temporal decompositions

Environmental Health ◽

10.1186/s12940-019-0544-9 ◽

2019 ◽

Vol 18 (1) ◽

Cited By ~ 4

Author(s):

Jacob S. Lefler ◽

Joshua D. Higbee ◽

Richard T. Burnett ◽

Majid Ezzati ◽

Nathan C. Coleman ◽

...

Keyword(s):

Air Pollution ◽

Particulate Matter ◽

Mortality Risk ◽

Air Pollutants ◽

Proportional Hazards ◽

Spatial Scales ◽

Fine Particulate Matter ◽

Coarse Fraction ◽

Cox Proportional Hazards ◽

Increased Risk

Abstract Background Cohort studies have documented associations between fine particulate matter air pollution (PM2.5) and mortality risk. However, there remains uncertainty regarding the contribution of co-pollutants and the stability of pollution-mortality associations in models that include multiple air pollutants. Furthermore, it is unclear whether the PM2.5-mortality relationship varies spatially, when exposures are decomposed according to scale of spatial variability, or temporally, when effect estimates are allowed to change between years. Methods A cohort of 635,539 individuals was compiled using public National Health Interview Survey (NHIS) data from 1987 to 2014 and linked with mortality follow-up through 2015. Modelled air pollution exposure estimates for PM2.5, other criteria air pollutants, and spatial decompositions (< 1 km, 1–10 km, 10–100 km, > 100 km) of PM2.5 were assigned at the census-tract level. The NHIS samples were also divided into yearly cohorts for temporally-decomposed analyses. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) in regression models that included up to six criteria pollutants; four spatial decompositions of PM2.5; and two- and five-year lagged mean PM2.5 exposures in the temporally-decomposed cohorts. Meta-analytic fixed-effect estimates were calculated using results from temporally-decomposed analyses and compared with time-independent results using 17- and 28-year exposure windows. Results In multiple-pollutant analyses, PM2.5 demonstrated the most robust pollutant-mortality association. Coarse fraction particulate matter (PM2.5–10) and sulfur dioxide (SO2) were also associated with excess mortality risk. The PM2.5-mortality association was observed across all four spatial scales of PM2.5, with higher but less precisely estimated HRs observed for local (< 1 km) and neighborhood (1–10 km) variations. In temporally-decomposed analyses, the PM2.5-mortality HRs were stable across yearly cohorts. The meta-analytic HR using two-year lagged PM2.5 equaled 1.10 (95% CI 1.07, 1.13) per 10 μg/m3. Comparable results were observed in time-independent analyses using a 17-year (HR 1.13, CI 1.09, 1.16) or 28-year (HR 1.09, CI 1.07, 1.12) exposure window. Conclusions Long-term exposures to PM2.5, PM2.5–10, and SO2 were associated with increased risk of all-cause and cardiopulmonary mortality. Each spatial decomposition of PM2.5 was associated with mortality risk, and PM2.5-mortality associations were consistent over time.

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Residential exposure to air pollution, access to neighborhood greenspace and their association with hair cortisol concentrations in the second and third trimester of pregnancy

10.21203/rs.3.rs-33256/v1 ◽

2020 ◽

Author(s):

Veerle Josefa Verheyen ◽

Sylvie Remy ◽

Nathalie Lambrechts ◽

Eva Govarts ◽

Ann Colles ◽

...

Keyword(s):

Air Pollution ◽

Stress Response ◽

Pregnancy Outcomes ◽

Major Road ◽

Second Trimester ◽

Hair Cortisol ◽

Third Trimester ◽

Residential Exposure ◽

Biological Stress ◽

Residential Distance

Abstract Background: Exposure to air pollution during pregnancy has been associated with adverse pregnancy outcomes in studies worldwide, other studies have described beneficial effects of residential greenspace on pregnancy outcomes. The biological mechanisms that underlie these associations are incompletely understood. Recent studies have shown that a biological stress response, with release of cortisol, may underlie associations between air pollution and health effects. The available research on air pollution exposure in relation to biological stress during pregnancy is still scarce. Methods: We explored associations between residential exposure to air pollution, access to neighborhood greenspace and hair cortisol concentrations in a prospective pregnancy cohort study. We modelled participants’ residential air pollutant concentrations (particulate matter with an aerodynamic diameter ≤ 2.5 μm, nitrogen dioxide (NO2), black carbon (BC)), assessed residential distance to a major road and access to a neighborhood greenspace. Hair cortisol concentrations, reflecting cortisol secretion over a period of 3 months prior to sampling, were determined at the end of the second (n = 133) and third pregnancy trimester (n = 81). Results: Three-month mean residential NO2 and BC concentrations were positively associated with third pregnancy trimester hair cortisol concentrations. The residential distance to a major road was negatively associated with second and third trimester hair cortisol concentrations. Access to a greenspace of 10 hectares or more within 800 meters travel distance significantly moderated the association between residential proximity to a major road and second trimester hair cortisol concentrations. At an average residential distance of 304 meters from a major road, mean second trimester HCC were estimated 22% lower for mothers with access to a neighborhood greenspace (3.71 (95% CI: 3.24, 4.24) pg/mg hair) compared to mothers without access (4.22 (95% CI: 3.26, 5.47) pg/mg hair). The moderation tended towards significance in the third trimester (p < 0.10). Conclusions: Increased residential exposure to air pollution and closer proximity to a major road are associated with an increased biological stress response in the second and third trimester of pregnancy, access to neighborhood greenspace may moderate the association. Trial registration: The IPANEMA study is registered under number NCT02592005 at clinicaltrials.gov.

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Interaction of Sirtuin 1 (SIRT1) candidate longevity gene and particulate matter (PM2.5) on all-cause mortality: a longitudinal cohort study in China

Environmental Health ◽

10.1186/s12940-021-00718-x ◽

2021 ◽

Vol 20 (1) ◽

Author(s):

Yao Yao ◽

Linxin Liu ◽

Guang Guo ◽

Yi Zeng ◽

John S. Ji

Keyword(s):

Air Pollution ◽

Particulate Matter ◽

Proportional Hazards ◽

Experimental Studies ◽

Cox Proportional Hazards ◽

Sirtuin 1 ◽

Environment Interaction ◽

Gene Environment ◽

Minor Alleles ◽

All Cause Mortality

Abstract Background The SIRT1 gene was associated with the lifespan in several organisms through inflammatory and oxidative stress pathways. Long-term air particulate matter (PM) is detrimental to health through the same pathways. Methods We used the Chinese Longitudinal Healthy Longevity Survey (CLHLS) to investigate whether there is a gene-environment (G × E) interaction of SIRT1 and air pollution on mortality in an older cohort in China. Among 7083 participants with a mean age of 81.1 years, we genotyped nine SIRT1 alleles for each participant and assessed PM2.5 concentration using 3-year average concentrations around each participant’s residence. We used Cox-proportional hazards models to estimate the independent and joint effects of SIRT1 polymorphisms and PM2.5 exposure on all-cause mortality, adjusting for a set of confounders. Results There were 2843 deaths over 42,852 person-years. The mortality hazard ratio (HR) and 95% confidence interval (CI) for each 10 μg/m3 increase in PM2·5 was 1.08 (1.05–1.11); for SIRT1_391 was 0.77 (0.61, 0.98) in the recessive model after adjustment. In stratified analyses, participants carrying two SIRT1_391 minor alleles had a significantly higher HR for each 10 μg/m3 increase in PM2.5 than those carrying zero minor alleles (1.323 (95% CI: 1.088, 1.610) vs. 1.062 (1.028, 1.096) p for interaction = 0.03). Moreover, the interaction of SIRT1 and air pollution on mortality is significant among women but not among men. We did not see significant relationships for SIRT1_366, SIRT1_773, and SIRT1_720. Conclusion We found a gene-environment interaction of SIRT1 and air pollution on mortality, future experimental studies are warranted to depict the mechanism observed in this study.

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Traffic-Related Air Pollution and Incident Dementia: Direct and Indirect Pathways Through Metabolic Dysfunction

Advances in Alzheimer’s Disease - Alzheimer’s Disease and Air Pollution ◽

10.3233/aiad210009 ◽

2021 ◽

Author(s):

Kimberly C. Paul ◽

Mary Haan ◽

Yu Yu ◽

Kosuke Inoue ◽

Elizabeth Rose Mayeda ◽

...

Keyword(s):

Air Pollution ◽

Mediation Analysis ◽

Mexican Americans ◽

Proportional Hazards ◽

Ambient Air ◽

Cox Proportional Hazards ◽

Ambient Air Pollution ◽

Metabolic Dysfunction ◽

Epidemiologic Evidence ◽

Incident Dementia

Background: Ambient air pollution exposure has been associated with dementia. Additionally, epidemiologic evidence supports associations between air pollution and diabetes as well as diabetes and dementia. Thus, an indirect pathway between air pollution and dementia may exist through metabolic dysfunction. Objective: To investigate whether local traffic-related air pollution (TRAP) influences incident dementia and cognitive impairment, non-dementia (CIND) in a cohort of older Mexican Americans. We also assess how much of this estimated effect might be mediated through type 2 diabetes (T2DM). Methods: In a 10-year, prospective study of Latinos (n = 1,564), we generated TRAP-NOx as a surrogate for pollution from local traffic sources at participants’ residences during the year prior to enrollment. We used Cox proportional hazards modeling and mediation analysis to estimate the effects of TRAP-NOx on dementia and/or CIND and indirect pathways operating through T2DM. Results: Higher TRAP-NOx was associated with incident dementia (HR = 1.55 for the highest versus lower tertiles, 95% CI = 1.04, 2.55). Higher TRAP-NOx was also associated with T2DM (OR = 1.62, 95% CI = 1.27, 2.05); furthermore, T2DM was associated with dementia (HR = 1.94, 95% CI = 1.42, 2.66). Mediation analysis indicated that 20% of the estimated effect of TRAP-NOx on dementia/CIND was mediated through T2DM. Conclusion: Our results suggest that exposure to local traffic-related air pollution is associated with incident dementia. We also estimated that 20% of this effect is mediated through T2DM. Thus, ambient air pollution might affect brain health via direct damage as well as through indirect pathways related to diabetes and metabolic dysfunction.

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Interaction of Sirtuin 1 (SIRT1) Candidate Longevity Gene and Particulate Matter (PM2.5) on All-cause Mortality: a Longitudinal Cohort Study in China

10.21203/rs.3.rs-77022/v1 ◽

2020 ◽

Author(s):

Yao Yao ◽

Linxin Liu ◽

Guang Guo ◽

Yi Zeng ◽

John S. Ji

Keyword(s):

Air Pollution ◽

Particulate Matter ◽

Proportional Hazards ◽

Recessive Model ◽

Cox Proportional Hazards ◽

Sirtuin 1 ◽

Environment Interaction ◽

Healthy Longevity ◽

Gene Environment ◽

All Cause Mortality

Abstract BackgroundThe SIRT1 gene was associated with the lifespan in several organisms through inflammatory and oxidative stress pathways. Long-term air particulate matter (PM) is detrimental to health through the same pathways. MethodsWe used the Chinese Longitudinal Healthy Longevity Survey (CLHLS) to investigate whether there is a gene-environment (G×E) interaction of SIRT1 and air pollution on mortality in an older cohort in China. Among 7,083 participants with a mean age of 81.1 years, we genotyped the SIRT1 alleles for each participant and assessed PM2.5 concentration using 3-year average concentrations around each participant's residence. We used Cox-proportional hazards models to estimate the independent and joint effects of SIRT1 polymorphisms and PM2.5 exposure on all-cause mortality, adjusting for a set of confounders. ResultsThere were 2,843 deaths over 42,852 person-years. The mortality hazard ratio (HR) and 95% confidence interval (CI) for each 10 μg/m³ increase in PM2·5 was 1.08 (1.05-1.11); for SIRT1_391 was 0.77 (0.61, 0.98) in the recessive model after adjustment. In stratified analyses, participants carrying two SIRT1_391 minor alleles had a significantly higher HR for each 10 μg/m³ increase in PM2.5 than those carrying one or none minor allele (1.336 [1.079-1.653] vs. 1.078 [1.049-1.107]; p for interaction = 0.012). Moreover, the interaction of SIRT1 and air pollution on mortality is significant among women but not among men. We did not see significant relationships for SIRT1_366, SIRT1_773, and SIRT1_720. ConclusionWe found a gene-environment interaction of SIRT1 and air pollution on mortality, possibly through the inflammation modulating mechanism of SIRT1 polymorphisms.

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Benefits of physical activity not affected by air pollution: a prospective cohort study

International Journal of Epidemiology ◽

10.1093/ije/dyz184 ◽

2019 ◽

Vol 49 (1) ◽

pp. 142-152 ◽

Cited By ~ 10

Author(s):

Shengzhi Sun ◽

Wangnan Cao ◽

Hong Qiu ◽

Jinjun Ran ◽

Hualiang Lin ◽

...

Keyword(s):

Physical Activity ◽

Air Pollution ◽

Hong Kong ◽

Tai Chi ◽

Proportional Hazards ◽

Cox Proportional Hazards ◽

P Value ◽

Additive Interaction ◽

Respiratory Mortality

Abstract Background Physical activity (PA) is beneficial to human health, whereas long-term exposure to air pollution is harmful. However, their combined effects remain unclear. We aimed to estimate the combined (interactive) mortality effects of PA and long-term exposure to fine particulate matter (PM2.5) among older adults in Hong Kong. Methods Participants aged ≥65 years from the Elderly Health Service Cohort (n = 66 820) reported their habitual PA at baseline (1998–2001) and were followed up till 31 December 2011. We used a satellite-based spatiotemporal model to estimate PM2.5 concentration at the residential address for each participant. We used Cox proportional hazards regression to assess the interaction between habitual PA and long-term exposure to PM2.5 on cardiovascular and respiratory mortality. We tested for additive interaction by estimating relative excess risk due to interaction and multiplicative interaction employing P-value for the interaction term. Results The death risks were inversely associated with a higher volume of PA and were positively associated with long-term exposure to PM2.5. The benefits of PA were more pronounced for participation in traditional Chinese exercise (e.g. Tai Chi) and aerobic exercise (e.g. cycling). We found little evidence of interaction between PA (volume and type) and long-term exposure to PM2.5 on either additive or multiplicative scales. Conclusions In this cohort of older Chinese adults, PA may decrease the risk of mortality, be it in areas of relatively good or bad air quality. The beneficial mortality effects of habitual PA outweighed the detrimental effects of long-term exposure to air pollution in Hong Kong.

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Association of Exposure to Hydrocarbons Air Pollution with Incidence of Atopic Dermatitis in Children

10.21203/rs.3.rs-93979/v1 ◽

2020 ◽

Author(s):

Chieh Wang ◽

Jeng-Dau Tsai ◽

Lei Wan ◽

Cheng-Li Lin ◽

Chang-Ching Wei

Keyword(s):

Air Pollution ◽

Atopic Dermatitis ◽

Proportional Hazards ◽

Incidence Rates ◽

Cox Proportional Hazards ◽

Air Pollutant ◽

Research Database ◽

Cox Proportional Hazards Models ◽

Increased Risk ◽

Taiwan National Health Insurance

Abstract Background:There is growing evidence that air pollution may act as an important environmental risk factor in the development and aggravation of childhood atopic dermatitis (AD). Methods:We collected data from the Taiwan National Health Insurance research database and linked the data to the Taiwan Air Quality-Monitoring Database. Children younger than 18 years old between January 1st, 2000 and until the diagnosis of AD was made, or December 31st, 2012, were selected from the database. We measured the incidence rate and hazard ratios for AD, and stratified by quartiles (Q1-Q4) of air pollutant concentration. Multivariable Cox proportional hazards models were also applied by adjusting for age, sex, monthly income, and level of urbanization. Results:Compared with those exposed to the concentrations in the Q1 quartile, the adjusted hazard ratio (HR) for AD increased, and total hydrocarbon (THC), non-methane hydrocarbon (NMHC), and methane (CH4) exposure concentrations ranged from 1.65 to 10.6, from 1.14 to 2.47, and from 1.70 to 11.9, respectively. Patients exposed to higher levels of THC, NMHC, and CH4 had greater accumulative incidence rates of childhood AD. Conclusions:The current study demonstrated that exposure to higher concentrations of THC, NMHC, and CH4 were associated with an increased risk of childhood AD.

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Incident cardiovascular disease and particulate matter air pollution in South Korea using a population-based and nationwide cohort of 0.2 million adults

Environmental Health ◽

10.1186/s12940-020-00671-1 ◽

2020 ◽

Vol 19 (1) ◽

Author(s):

Ok-Jin Kim ◽

Soo Hyun Lee ◽

Si-Hyuck Kang ◽

Sun-Young Kim

Keyword(s):

Cardiovascular Disease ◽

Air Pollution ◽

Particulate Matter ◽

South Korea ◽

Proportional Hazards ◽

Population Based ◽

Average Concentration ◽

Cox Proportional Hazards ◽

High Dose

Abstract Background While many studies reported the association between long-term exposure to particulate matter air pollution (PM) and cardiovascular disease (CVD), few studies focused on incidence with relatively high-dose exposure using a nationwide cohort. This study aimed to investigate the association between long-term exposure to PM10 and PM2.5 and incidence of CVD in a nationwide and population-based cohort in South Korea where the annual average concentration of PM2.5 is above 20 μg/m3. Methods We selected 196,167 adults in the National Health Insurance Service-National Sample Cohort (NHIS-NSC) constructed based on the entire South Korean population. Incidence of four CVD subtypes including ischemic heart disease (IHD), myocardial infarction, heart failure, and stroke, and total CVD including all four was identified as the first diagnosis for 2007–2015. To assess individual exposures, we used annually-updated district-level residential addresses and district-specific PM concentrations predicted by a previously developed universal kriging prediction model. We computed individual-level long-term PM concentrations for four exposure windows: previous 1, 3, and 5 year(s) and 5 years before baseline. We applied time-dependent Cox proportional hazards models to estimate hazard ratios (HRs) of incident CVDs per 10 μg/m3 increase in PM10 and PM2.5 after adjusting for individual- and area-level characteristics. Results During 1,578,846 person-year, there were 33,580 cases of total incident CVD. Average PM10 and PM2.5 concentrations for the previous 5 years were 52.3 and 28.1 μg/m3, respectively. A 10 μg/m3 increase in PM2.5 exposed for the previous 5 years was associated with 4 and 10% increases in the incidence of total CVD (95% confidence interval: 0–9%) and IHD (4–16%), respectively. HRs tended to be higher with earlier exposure for IHD and more recent exposure for stroke. The estimated shape of the concentration-response relationship showed non-linear patterns. We did not find evidence of the association for PM10. Conclusions Using a population-based nationwide cohort exposed to relatively high PM concentration, this study confirmed the association between PM2.5 and CVD incidence that was reported in previous studies mostly with low-dose environments. The magnitude and the shape of the association were generally consistent with previous findings.

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Interaction of Sirtuin 1 (SIRT1) candidate longevity gene and particulate matter (PM2.5) on all-cause mortality: a longitudinal cohort study in China

10.21203/rs.3.rs-77022/v2 ◽

2021 ◽

Author(s):

Yao Yao ◽

Linxin Liu ◽

Guang Guo ◽

Yi Zeng ◽

John S. Ji

Keyword(s):

Air Pollution ◽

Particulate Matter ◽

Proportional Hazards ◽

Experimental Studies ◽

Cox Proportional Hazards ◽

Sirtuin 1 ◽

Environment Interaction ◽

Gene Environment ◽

Minor Alleles ◽

All Cause Mortality

Abstract Background The SIRT1 gene was associated with the lifespan in several organisms through inflammatory and oxidative stress pathways. Long-term air particulate matter (PM) is detrimental to health through the same pathways. Methods We used the Chinese Longitudinal Healthy Longevity Survey (CLHLS) to investigate whether there is a gene-environment (G×E) interaction of SIRT1 and air pollution on mortality in an older cohort in China. Among 7,083 participants with a mean age of 81.1 years, we genotyped nine SIRT1 alleles for each participant and assessed PM2.5 concentration using 3-year average concentrations around each participant's residence. We used Cox-proportional hazards models to estimate the independent and joint effects of SIRT1 polymorphisms and PM2.5 exposure on all-cause mortality, adjusting for a set of confounders. Results There were 2,843 deaths over 42,852 person-years. The mortality hazard ratio (HR) and 95% confidence interval (CI) for each 10 μg/m³ increase in PM2·5 was 1.08 (1.05-1.11); for SIRT1_391 was 0.77 (0.61, 0.98) in the recessive model after adjustment. In stratified analyses, participants carrying two SIRT1_391 minor alleles had a significantly higher HR for each 10 μg/m³ increase in PM2.5 than those carrying zero minor alleles (1.323 (95% CI: 1.088, 1.610) vs. 1.062 (1.028, 1.096) p for interaction = 0.03). Moreover, the interaction of SIRT1 and air pollution on mortality is significant among women but not among men. We did not see significant relationships for SIRT1_366, SIRT1_773, and SIRT1_720. Conclusion We found a gene-environment interaction of SIRT1 and air pollution on mortality, future experimental studies are warranted to depict the mechanism observed in this study.

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